Controlled clinical trials have shown that tripotassium dicitrato bismuthate healed duodenal and gastric ulcers significantly better than placebo. One mechanism suggested is that it forms a protective coat at the ulcer base. We studied this coating action in rats with chronic gastric ulcers produced by a standardized technique for mucosal wounding at the fundoantral junction. Bismuth was identified by histochemical staining using Castel's reagent, the specificity of which was verified in vitro against 13 other metallic compounds and chemicals. Our results showed that tripotassium dicitrato bismuthate had a coating affinity for the ulcer base, but not for the adjacent normal mucosa. All rats treated with tripotassium dicitrato bismuthate 1, 2, 4, and 6 h previously, but not the control rats treated with water or those treated with four other bismuth compounds, manifested a layer of bismuth that coated the ulcer base. Light and electron microscopy of the tripotassium dicitrato bismuthate-treated ulcers--but not their controls-revealed an abundance of macrophages, which had ingested the bismuth. This unique bismuth coat may insulate the ulcer base from acid-pepsin digestion, while the influx of macrophages may expedite reparative processes.